Pneumocystis Jirovecii

As a leading company in the field of biological research and drug discovery, Creative Biolabs has gained a wealth of good reputation for successfully completed numerous challenges in antifungal drug discovery. Based on our advanced technology platform and experienced scientists, we are able to provide a series of antifungal drug discovery services against various fungal diseases and related fungi. Here, we describe a pathogenic fungus Pneumocystis Jirovecii that can cause pneumocystis pneumonia.

Introduction

Pneumocystis Jirovecii (P. Jirovecii), also known as Pneumocystis carinii previously, is a yeast-like fungal organism that typically causes pneumocystis pneumonia infections in immunocompromised patients. It belongs to genus Pneumocystis, family Pneumocystidaceae, order Pneumocystidales, class Pneumocystidomycetes, and phylum Ascomycota. Currently, there are five species have been identified: P. carinii and P. wakefieldiae in rats, P. murina in mice, P. oryctolagi in rabbits, and P. jirovecii in humans. P. Jirovecii is an unusual ascomycetous fungus that can be detected in the lungs of both healthy individuals and immunocompromised patients.

This fungus is commonly transmitted via the air from infected individuals to new hosts, also possibly by the transplacental route. P. Jirovecii is a unicellular eukaryotic organism that inhabits in the lung of human beings, which cannot be cultured in vitro. It was originally discovered in 1906 by Carlos Chagas and was initially considered to be a protozoan. Recent investigations demonstrated that the organism is now considered to be a fungus rather than a protozoan.

Pathogenesis of P. Jirovecii

P. jirovecii is the only causative agent for human, particularly for those who with HIV or AIDS, transplant operation, hematologic malignancies, and immunodeficiencies. P. jirovecii usually parasitizes in alveoli after invading human lungs. Subsequently, adhesion and proliferation of the fungus on the surface of alveolar epithelial cells cause inflammatory reactions. Pulmonary alveoli are permeated a great number of foam exudates, which contain tissue cells, lymphocytes, plasma cells, and accumulated trophozoites and cysts. Gradually, more and more P. jirovecii and exudates accumulate continuously, block pulmonary alveoli and bronchioles, which leading to pulmonary ventilation dysfunction even respiratory failure and death.

Fig.1 P. jirovecii cysts in tissue.

Lifecycle of P. Jirovecii

P. Jirovecii has a biphasic life cycle with two distinct morphological forms: the haploid trophozoite form and the cyst form. Both trophozoite form and the cyst form all occur only inside the host's lungs.

• Trophozoite form, also named trophic form, is single-celled and thought to multiply through asexual binary fission, which represents the large majority of the total P. Jirovecii population. The trophic form of P. Jirovecii tightly adheres to the type I pneumocytes of the alveolar epithelium in the host, which is predominate in lungs during the infection.
• The cyst form is generated through the conjugation of two opposite mating type trophic forms via sexual reproduction. A cyst contains eight nuclei after mature, then ruptures and releases eight ascospores (trophic forms) from the intracystic nuclei. The cyst form represents a reproductive stage, which plays an important role in the propagation and transmission of P. Jirovecii.

Fig.2 Schematic overview of the life cycle of P. Jirovecii. (Schildgen, 2014)

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Reference

1. Schildgen, V.; et al. Pneumocystis jirovecii can be productively cultured in differentiated CuFi-8 airway cells. Mbio. 2014, 5(3): 01186-14.

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